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Clin. Cardiol. 25, 33-37 (2002)
Ryan V. Cantwell, M.D., Ronnier J. Aviles, M.D., Johannes Bjornsson, M.D.,* R. Scott Wright, M.D.,† William K. Freeman, M.D.,† Jae K. Oh, M.D.,† James D. Hoyer, M.D.,* Svetomir Markovic, M.D., Allan S. Jaffe, M.D.*†
Mayo Clinic and Foundation, Departments of Internal Medicine and *Laboratory Medicine and Pathology, and †Division of Cardiology, Rochester, Minnesota, USA
Summary: We present the case of a 43-year-old male who was initially evaluated for angina pectoris and dyspnea. His CK, CK-MB, and cTnI were all elevated following a blood transfusion and he underwent coronary arteriography, which demonstrated no luminal obstructions. After several months, he was transferred to Mayo Clinic where diagnoses of fulminant cardiac amyloidosis and systemic multiple myeloma were established. The cTnI remained elevated despite normalization of the CK and CK-MB. Despite aggressive treatment, the patient died. Postmortem analysis demonstrated amyloid cardiac deposition including involvement of the coronary microvasculature. Electron microscopy revealed myocyte compression injury from amyloid infiltration. We believe this is the first report of elevated troponin I in a patient with cardiac amyloidosis. The electron microscopy in our case confirms cardiac damage as the mechanism for cTnI elevation. This observation strengthens our knowledge about the specificity of cTnI for the detection of cardiac injury.
Key words: troponin, cardiac amyloidosis, angina pectoris, myocardial infarction
Address for reprints:
R. Scott Wright, M.D.
Division of Cardiovascular Diseases, Mayo Clinic
200 First Street SW
Rochester, MN 55905, USA
e-mail: wright.scott@mayo.edu
Received: December 14, 1999
Accepted with revision: February 2, 2000